The expression profile of ABC transporter genes in post-treatment breast carcinomas
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43807 | GEO | 2013/03/01
SECONDARY ACCESSION(S): PRJNA187483
REPOSITORIES: GEO
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Project description:ATP-binding cassette (ABC) transporters contribute to development of resistance to anti-cancer drugs via ATP-dependent drug efflux. A major goal of our study was to investigate associations between expression of ABC transporters and outcome of breast carcinoma patients. ABCA5/6/8/9/10, ABCB1/5/11, ABCC6/9, ABCD2/4 and ABCG5/G8 were significantly downregulated and ABCA2/3/7/12, ABCB2/3/8/9/10, ABCC1/4/5/10/11/12, ABCD1/3, ABCE1, ABCF1/2/3 and ABCG1 upregulated in post-treatment tumors compared with non-neoplastic tissues. Significant associations of ABCC1 and ABCC8 levels in tumors with grade and expression of hormonal receptors were found. ABCA13 and ABCD2 levels significantly associated with the response to neoadjuvant chemotherapy in post-treatment patients. Transcript levels of all forty nine human ABCs were determined by qPCR in post-treatment tumor and non-neoplastic tissue samples from 68 breast carcinoma patients treated by neoadjuvant chemotherapy. EIF2B1, MRPL19, IPO8, and UBB were used as reference genes for data normalization.
2013-03-01 | E-GEOD-43807 | biostudies-arrayexpress
Project description:The ATP binding cassette (ABC) transporter family is widely distributed in vertebrates and is essential for drug resistance, cell signaling and energy homeostasis. There is growing evidence that various ABC transporters contribute to the growth and development of tumors but relatively little is known about how the ABC transporter family behaves in hepatocellular carcinoma (HCC). ABCC6 transporter was downregulated in HCC tissues and that it was associated with successful treatment for HCC patients. Cellular model studies have shown that ABCC6 plays a role in the migration and cytoskeleton rearrangement of HepG2 hepatocarcinoma cells, highlighting its role in cancer biology. Abcc6-silenced HepG2 cells are used as cell model to obtain more deep information about the molecular mechanisms underlying the observed results. MTT and colony formation assays, showed the effects of Abcc6 on HepG2 cell proliferation. Western blotting analysis, real-time PCR, and immunofluorescence were used to find the E-cadherin, Vimentin, and N-cadherin markers associated with the epithelial-to-mesenchymal transition (EMT). Colony formation experiments in the current study showed that Abcc6 decreased HepG2 cell viability. The migratory and invasion activities were dramatically slowed down by Abcc6 silencing, according to the Transwell and wound-healing assays. In tumor cells, EMT has been shown to be crucial for enhancing migration and invasion and is frequently characterized by a loss of epithelial markers (E-cadherin) and an increase in mesenchymal markers (Vimentin and N-cadherin). In the western blotting examination, E-cadherin expression was considerably elevated compared to the control group, while N-cadherin and Vimentin expression were downregulated. This led to the hypothesis that the underlying mechanism of Abcc6 knockdown prevents migration and invasion in HepG2 cells and is linked to the suppression of EMT. In conclusion all evidence suggested that ABC transporters play a more active role in cancer biology.
2024-01-02 | E-MTAB-13154 | biostudies-arrayexpress
Project description:Krohn2011 - Cerebral amyloid-β
proteostasis regulated by membrane transport protein ABCC1
This model is described in the article:
Cerebral amyloid-β
proteostasis is regulated by the membrane transport protein
ABCC1 in mice.
Krohn M, Lange C, Hofrichter J,
Scheffler K, Stenzel J, Steffen J, Schumacher T, Brüning T,
Plath AS, Alfen F, Schmidt A, Winter F, Rateitschak K, Wree A,
Gsponer J, Walker LC, Pahnke J.
J. Clin. Invest. 2011 Oct; 121(10):
3924-3931
Abstract:
In Alzheimer disease (AD), the intracerebral accumulation of
amyloid-β (Aβ) peptides is a critical yet poorly understood
process. Aβ clearance via the blood-brain barrier is reduced by
approximately 30% in AD patients, but the underlying mechanisms
remain elusive. ABC transporters have been implicated in the
regulation of Aβ levels in the brain. Using a mouse model of AD
in which the animals were further genetically modified to lack
specific ABC transporters, here we have shown that the
transporter ABCC1 has an important role in cerebral Aβ
clearance and accumulation. Deficiency of ABCC1 substantially
increased cerebral Aβ levels without altering the expression of
most enzymes that would favor the production of Aβ from the Aβ
precursor protein. In contrast, activation of ABCC1 using
thiethylperazine (a drug approved by the FDA to relieve nausea
and vomiting) markedly reduced Aβ load in a mouse model of AD
expressing ABCC1 but not in such mice lacking ABCC1. Thus, by
altering the temporal aggregation profile of Aβ,
pharmacological activation of ABC transporters could impede the
neurodegenerative cascade that culminates in the dementia of
AD.
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2016-07-27 | BIOMD0000000618 | BioModels
Project description:The airway epithelium represents a critical component of the human lung that helps orchestrate defences against respiratory tract viral infections, which are responsible for more than 2.5 million deaths/year globally. Innate immune activities of the airway epithelium rely Toll-like receptors (TLRs), nucleotide binding and leucine-rich-repeat pyrin domain containing (NLRP) receptors, and cytosolic nucleic acid sensors. ATP Binding Cassette (ABC) transporters are ubiquitous across all three domains of life – Archaea, Bacteria, and Eukarya – and expressed in the human airway epithelium. ABCF1, a unique ABC family member that lacks a transmembrane domain, has been defined as a cytosolic nucleic acid sensor that regulates CXCL10, interferon-b expression, and downstream type I interferon responses. We tested the hypothesis that ABCF1 functions as a dsDNA nucleic acid sensor in human airway epithelial cells important in regulating antiviral responses.
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Project description:Irinotecan (CPT-11) is now widely used as the first-line chemotherapy for mCRC. There were 4 key enzymes for CPT-11 metabolizing, CYP3A4, UDP-glucuronosyltransferase, carboxylesterase(CES), and ATP-binding cassette (ABC) transporters. Genetic variations of those enzymes may cause the heterogeneity in safety and efficacy of CPT-11. The aim of this study is to figure out the correlation between the genetic polymorphism and the drug response.
| 2101269 | ecrin-mdr-crc
Project description:Being the most malignant disease among females, breast cancer has morbidity and mortality in the first and second positions among various cancers [1]. Up to now, chemotherapy has been the most common therapy [2]; however, multidrug resistance (MDR) often occurs to give low overall survival rate. Thus, it is urgent to figure out the mechanism of chemotherapy resistance. The first step of drugs to attack tumor cells is to interact with the plasma membrane, and solute carrier (SLC) family proteins are uptake transporters [3]. On the other side, the efflux transporters (such as ATP-binding cassette, ABC) pump drug out of cancer cells [4]. The main mechanism of MDR is the upregulation of ATP-binding cassette (ABC) transporters [5]. Breast cancer resistance protein (ABCG2), multidrug resistance protein (ABCC1) and P-glycoprotein (P-gp) have been extensively studied [6,7]. Formation of CSCs [8], DNA damage [9] and cell apoptosis [10] and epithelial mesenchymal transition (EMT) are other mechanisms of MDR. To zoom in on the correlation between altered glycosylation and drug resistance and to find out the putative biomarkers, MS-based glycoprotomics is a method of choice. Here, we report our N-glycoproteomics study of differential N-glycosylation from the whole cell lysate of MCF-7/ADR CSCs (adriamycin-resistant MCF-7 CSCs) relative to MCF-7 CSCs. Intact N-glycopeptides from both cells were enriched with ZIC-HILIC, isotopically diethylated, mixed with 1:1 ratio, and the mixture was analyzed by C18-RPLC-ESI-MS/MS (HCD with stepped NCE). Differentially expressed N-glycopeptides (DEGPs) were identified and quantified with database search using GPSeeker.
2023-07-04 | PXD036095 | Pride
Project description:This study investigated the biological function of ABCB7 in U87MG glioblastoma cell line. Many ABC transporters are known contributions to drug resistance and various biological process. However, mitochondrial ABC transporters aren’t known mechanism to control biological process. We identified the potential roles of ATP-binding cassette (ABC) transporter subfamily member 7 (ABCB7), one of the mitochondrial ABC transporters. ABCB7 activates signaling pathway of hypoxia-inducible factor 1 alpha (HIF1α) by hypoxia independent regulation. This signaling pathway regulates the death inhibitory genes and survival related genes. Also, ABCB7 downregulates cell cycle related genes. Our results provide that ABCB7 is essential for the survival of malignant brain tumors.
2020-01-01 | GSE120627 | GEO
Project description:ATP-binding cassette (ABC) transporters can translocate a broad spectrum of molecules across the cell membrane including physiological cargo and toxins. ABC transporters are known for the role they play in resistance towards anticancer agents in chemotherapy of cancer patients. There are 68 ABC transporters annotated in the genome of the social amoeba Dictyostelium discoideum. We have characterized more than half of these ABC transporters through a systematic study of mutations in their genes. We have analyzed morphological and transcriptional phenotypes for these mutants during growth and development and found that most of the mutants exhibited rather subtle phenotypes. A few of the genes may share physiological functions, as reflected in their transcriptional phenotypes. Since most of the abc-transporter mutants showed subtle morphological phenotypes, we utilized these transcriptional phenotypes to identify genes that are important for development by looking for transcripts whose abundance was unperturbed in most of the mutants. We found a set of 668 genes that includes many validated D. discoideum developmental genes. We have also found that abcG6 and abcG18 may have potential roles in intercellular signaling during terminal differentiation of spores and stalks. Transcriptional phenotyping during development of abc transporter mutants in Dictyostelium discoideum
2013-06-14 | E-GEOD-45555 | biostudies-arrayexpress
Project description:Transcriptomic analysis of annulus fibrosus (AF) tissues from intervertebral discs of 7-month-old mice with the global deletion of ABCC6. ABCC6 is an efflux transporter of ATP in hepatic cells and loss of function results in metabolic ectopic mineralization disorder pseudoxanthoma elsaticum. To understand the role of ABCC6 and ectopic mineralization in the disc, we examined the transcriptomic profiles of annulus fibrosus cells in control and ABCC6 knock-out mice using microarrays.
2021-11-17 | GSE188943 | GEO
Project description:We reported the hepatic gene expression profiling in mice fed with a high fat diet compared to the controls. We found that the modulation of pathways related to peroxisome proliferator-activated receptors, cytochrome P450s, and ATP-binding cassette transporters in high fat diet mice. Particularly, constitutive androstane receptor and pregnane X receptor signature genes Cyp2b10 and Cyp3a11 were significantly increased in high fat diet mice compared to controls. Liver X receptor mediated Abcg5 and Abcg8 were also found increased by HFD treatment.
2018-08-28 | GSE118070 | GEO